AKT1 gene mutations occur with some frequency in cancer, particularly the one in the pleckstrin homology domain, Glu17Lys, which enhances its binding to the PI3K ligand and relocalization to the plasma membrane, intensifying cell migration and resistance to chemotherapeutic treatment in breast cancers, as well as selective destruction of chemotherapy-resistant tumor cells and those with low levels of AKT gene expression [75,76,77]. This evidence concerns the gene AKT1 and neoplasm.